The Implications Of The BMP-7 AND OP-1 Research On Intervertebral Disk Height

In a post I had written before which was entitled “Osteogenic Protein 1 OP-1 Or Bone Morphogenetic Protein 7 BMP-7 Can Increase Intervertebral Disk Height (Important)” I had shown that an injection of BMP-7 (aka OP-1) into the intervertebral disk nucleus pulposus resulted in vertebral height increase and disk regeneration.

At the time, I felt that the post was the most significant discovery of a possible way to increase height since the experiments on rabbits  who suffered disk degeneration was so effective. From just one injection of OP-1 the effect on disk regeneration and also disk height increase lasted for upwards of at least 2 weeks in all of the experiments.

What I was thinking at the time was moving from the rabbit model into the human subjects. If we took subjects who were suffering from disk degeneration and injected OP-1 into the their disks, would it result in long term effects or would we have to consistently over time keep on adding the OP-1. Plus, there were studies which showed that if you use a needle to punture the disk, you could cause complete lumbar collapse, disk lose, and other horrible problems.

Right now in my research, I was thinking of trying a more noninvasive approach which is to take capsules or implants which you can place around the said disk which has a semipermeable membrane which allows for the OP-1 to only diffuse in one direct from a concentration gradient. at this point I would guess that the intervertebral disk is made of a type of collagen fiber which is permeable. From my past with guages and biomedical application, I would be even willing to suggest trying out a patch or guass you can directly apply to your back side which can absorb the BMP-7 concentratin through the skin and reach the disk.

From this source HERE we learn that…

The discs in your spine are made up of the inner, gelatinous nucleus pulposus and the outer annulus fibrosus. This outer ring is a firm, ligament that encloses the spongey nucleus and prevents it from herniating or bulging beyond its normal perimeter, according to Jack Zigler, M.D. on the Spine-health website. The annulus also disperses the pressure on the vertebrae caused by weight-bearing activities. If the annular fibers stretch or tear, the nucleus can herniate, which may lead to back pain and sciatica.

From this source HERE we learn that…

ANNULUS FIBROSUS

The intervertebral disc is made up of two parts: the annulus fibrosus and the nucleus pulposus. The annulus fibrosus is the outer layer of the disc that encompasses the gel-like nucleus pulposus inside the disc. Made of strong layers of collagen fibers woven together at varying angles, the annulus fibrosus gives structure to the disc and allows for even weight distribution of surrounding vertebrae.

Though designed to endure relatively great amounts of pressure, over time the annulus fibrosus begins to lose flexibility and elasticity, leaving it vulnerable to damage. A weakened intervertebral disc can begin to “bulge,” causing a bubble of nucleus pulposus material to protrude in the outer layer. In some cases, a bulging disc can turn into a herniated disc, which is when the annulus fibrosus wall completely ruptures and releases nucleus material into the spinal canal. Depending on the amount of disc material placing pressure on the spinal cord and nerve roots, symptoms can range from mild to severe.

While intervertebral disc damage is often a result of aging and normal wear and tear to the spine, there are steps you can take to mitigate it. Exercising and maintaining a healthy body weight will help ensure your spine is adequately supported and decrease the amount of pressure placed on the annulus fibrosus of each disc. Since cigarette smoking decreases the amount of water in the discs, it can actually cause discs to degenerate faster, so you also should avoid smoking. Finally, maintaining correct posture and using proper body mechanics when lifting, exercising, or sleeping will minimize your chances of developing a disc problem.

This picture taken from Wikipedia link HERE .

What is important to note is that the back is not completely made of irregular vertebrate bone. There are the areas of disks which we might be able to manipulate.

The disk annulus is made of collagen fibers that seems to connect at an angle. The composition is a lot of water. If the disk is permeable of a certain we should be able to get salt into it using a concentration gradient, and then use water into the disk through another semipermeable gradient that only allows water to go through.

Osteogenic Protein 1 OP-1 Or Bone Morphogenetic Protein 7 BMP-7 Can Increase Intervertebral Disk Height (Important)

I had stated in a recent post that the BMPs were the most viable path to look into at this point of the research for a height increase technique. The studies and research have shown that this type of protein, which is in the family of TGF-β cellular proteins is very effective in spinal fusions of fractures.

Source 1 – Title “Intradiscal administration of osteogenic protein-1 increases intervertebral disc height and proteoglycan content in the nucleus pulposus in normal adolescent rabbits.”

Spine (Phila Pa 1976). 2005 Jan 1;30(1):25-31; discussion 31-2.

An HS, Takegami K, Kamada H, Nguyen CM, Thonar EJ, Singh K, Andersson GB, Masuda K.

Source
Department of Orthopedic Surgery, Rush Medical College at Rush University Medical Center, Chicago, Illinois, USA.

Abstract

STUDY DESIGN:
A study of the disc height and biochemical changes in the rabbit intervertebral disc after injection of osteogenic protein-1 into the nucleus pulposus.

OBJECTIVES:
To evaluate the in vivo effects of osteogenic protein-1 administered intradiscally to the intervertebral disc of rabbits.

SUMMARY OF BACKGROUND DATA:
Growth factors, such as osteogenic protein-1 and transforming growth factor-beta, have the ability to stimulate synthesis of proteoglycan and collagen in vitro. No attempts have yet been made to determine the effects of these growth factors in an in vivo model.

METHODS:

Twenty-four New Zealand adolescent white rabbits were divided evenly into two subject groups. In one group, three consecutive intervertebral discs were injected with saline; whereas in the other group, they were injected with osteogenic protein-1 in saline. At 2, 4, and 8 weeks after the injection, the intervertebral disc heights of the injected specimens were measured by lateral plain radiographs and compared with preinjection measurements. The change in disc height was expressed as the percent disc height index compared with the preinjection value. After the radiographic measurements were obtained, the intervertebral discs were removed and analyzed for DNA, proteoglycan, and collagen contents.

RESULTS:

At 2 weeks after the injections, the mean disc height index of the osteogenic protein-1-injected discs was 15% greater than that of the saline group. The increase in disc height with osteogenic protein-1 injection was still statistically significant at the 4- and 8-week time points. The proteoglycan content of the nucleus pulposus in discs injected with osteogenic protein-1 was higher than that in the saline group at the 2-week time point. The osteogenic protein-1-induced effect on the proteoglycan content was also present at the 4- and 8- week time intervals; however, these increases were not statistically significant. There were no significant differences in the DNA content, normalized to noninjected control, of the nucleus pulposus between the saline and osteogenic protein-1 groups. However, a significant increase in the DNA content of the anulus fibrosus in the osteogenic protein-1 group, compared with that of the anulus fibrosus in the saline group, was observed after 4 weeks.

CONCLUSION:

To date, no study has demonstrated the potential in vivo effects of growth factors on the intervertebral disc. The present study reports that the intradiscal administration of osteogenic protein-1 in vivo results in an increased disc height present at 2, 4, and 8 weeks and an increase in PG content of the nucleus pulposus at the 2-week time point. Therefore, osteogenic protein-1 may act to stimulate metabolic activity in the nucleus pulposus. Continued research is needed to evaluate the potential of growth factor-induced reversal of age-related disc degeneration in an appropriate animal model. In addition, studies in a nonhuman primate animal model will be essential before considering intradiscal injection of growth factors in humans.

PMID: 15626976       [PubMed – indexed for MEDLINE]

Source 2 – Title “Osteogenic protein-1 injection into a degenerated disc induces the restoration of disc height and structural changes in the rabbit anular puncture model.

Spine (Phila Pa 1976). 2006 Apr 1;31(7):742-54.

K, Imai Y, Okuma M, Muehleman C, Nakagawa K, Akeda K, Thonar E, Andersson G, An HS.

Source
Department of Orthopedic Surgery, Rush Medical College at Rush University Medical Center, Chicago, IL, USA. kmasuda@rush.edu

Abstract

STUDY DESIGN:
In vivo study of the effect of injection of osteogenic protein-1 (OP-1) on a rabbit anular needle puncture model of intervertebral disc (IVD) degeneration.

OBJECTIVE:
To study radiographic, magnetic resonance imaging (MRI), biochemical, and histologic changes in the rabbit IVD after injection of OP-1 into the nucleus pulposus in a needle puncture disc degeneration model.

SUMMARY OF THE BACKGROUND DATA:
Growth factors, such as OP-1, have the ability to stimulate synthesis of proteoglycans and collagen in vitro. The in vivo injection of OP-1 into the normal rabbit IVD has increased disc height and proteoglycan content in the anulus fibrosus and nucleus pulposus. However, to our knowledge, no attempts have yet been made to determine the effects of these growth factors in an in vivo model of disc degeneration.

METHODS:
New Zealand adolescent white rabbits (n = 90, 8 for baseline evaluation, 82 at 8 times) received an anular puncture in 2 noncontiguous discs with an 18-gauge needle to induce disc degeneration. Four weeks later, either 5% lactose (10 microL) or OP-1 (100 microg in 10 microL 5% lactose) was injected into the center of the nucleus pulposus. The disc height was followed radiographically for up to 24 weeks after the injections. At the 2, 4, 8, 12, and 24-week times after the injection, rabbits were euthanized, and MRI of the harvested spinal columns was obtained to grade the degeneration. The discs injected with OP-1 or lactose and noninjected discs were subjected to biochemical and histologic analysis. The specimens at the 24-week time were limited to histologic evaluation.

RESULTS:

The anular puncture with a needle induced a consistent disc narrowing within 4 weeks. The injection of OP-1 induced a restoration of disc height at 6 weeks, which was sustained for the entire experimental period, up to 24 weeks after the injection. The injection of lactose alone did not change the course of disc narrowing over the same time. MRI grading score showed significant differences between the OP-1 and lactose groups at the 8, 12, and 24-week times, suggesting an increase in water content in the nucleus pulposus of the OP-1 group. The proteoglycan content of the nucleus pulposus and anulus fibrosus was significantly higher in the OP-1 group than in the control group. The degeneration grades of the punctured discs in the OP-1 group were significantly lower than those in the lactose group.

CONCLUSION:

The results of this study show the feasibility of restoring degenerative rabbit discs by a single injection of OP-1 into the nucleus pulposus. Importantly, the effects of the OP-1 injection on disc height were sustained for up to 24 weeks. The metabolic changes in the cells, following a single injection, might be sustained and, thus, induce long-term changes in disc structure. An efficacy study in large animals is required to show further that the intradiscal injection of OP-1, or bone morphogenetic proteins or growth factors with similar properties would be useful for the structural restoration of the IVD in humans.

PMID: 16582847     [PubMed – indexed for MEDLINE]

Source 3 – Title “Restoration of disc height loss by recombinant human osteogenic protein-1 injection into intervertebral discs undergoing degeneration induced by an intradiscal injection of chondroitinase ABC.”

Spine (Phila Pa 1976). 2007 May 15;32(11):1197-205.

Restoration of disc height loss by recombinant human osteogenic protein-1 injection into intervertebral discs undergoing degeneration induced by an intradiscal injection of chondroitinase ABC.

Imai Y, Okuma M, An HS, Nakagawa K, Yamada M, Muehleman C, Thonar E, Masuda K.

Source<
Department of Orthopedic Surgery, Rush Medical College at Rush University Medical Center, Chicago, IL 60612, USA.

Abstract

STUDY DESIGN:

In vivo study of the effect of an injection of recombinant human osteogenic protein-1 into degenerated discs induced by chondroitinase ABC.

OBJECTIVE:

To investigate the efficacy of an injection of recombinant human osteogenic protein-1 to induce the recovery of disc height, and biochemical and histologic repair, in discs degenerated through enzymatic digestion by chondroitinase ABC.

SUMMARY OF THE BACKGROUND DATA:

Chondroitinase ABC is currently proposed as a chemonucleolysis agent; however, postchemonucleolysis degeneration is currently unavoidable. Recombinant human OP-1 has been shown to promote extracellular matrix repair in vitro and in vivo.

METHODS:

Fifty-four adolescent New Zealand white rabbits were used. Four weeks after an initial injection of chondroitinase ABC (10 mU/disc), 5% lactose (10 microL/disc) or recombinant human osteogenic protein-1 (100 microg in 10 microL lactose/disc) was injected. Disc heights were monitored radiographically at 2-week intervals, and rabbits were killed at 6, 8, 12, and 16 weeks after the initial chondroitinase ABC injections. The intervertebral discs were subjected to histologic and biochemical analyses.

RESULTS:

Significant disc space narrowing was observed in both groups 2 weeks after the injection of chondroitinase ABC. In the chondroitinase ABC/lactose group, this narrowing progressed after the vehicle injection and was sustained for up to 16 weeks. In the chondroitinase ABC/recombinant human osteogenic protein-1 group, the disc height index showed a significant increase at 6 weeks (lactose vs. recombinant human osteogenic protein-1; P < 0.01); this recovery was sustained for up to 16 weeks. The proteoglycan content was higher in the chondroitinase ABC/recombinant human osteogenic protein-1 group than in the chondroitinase ABC/lactose group. However, histologic changes, after the recombinant human osteogenic protein-1 injection, were not observed.

CONCLUSIONS:
A single injection of recombinant human osteogenic protein-1 into a rabbit disc dramatically reversed the decrease in disc height induced by chondroitinase ABC chemonucleolysis. The recovery was significant and sustained over the next 12 weeks. The therapeutic effects of both chondroitinase ABC chemonucleolysis and recombinant human osteogenic protein-1 injections should be further explored in higher animals before it is applied to humans.

PMID: 17495776     [PubMed – indexed for MEDLINE]

Me: Tyler from HeightQuest wrote a similar article HERE about the studies which shows the effects of using OP-1 aka BMP-7 on the intervertebral disk height.

What I am not sure of is the first passage which he takes. are the subjects in the experiment rabbits, sheep, or humans?? However, the results are very clear. using GDF-5 (I have got to do a post about this compound protein!!) and OP-1 injected into the disks increased the nucleus pulpous cell types and the collagen, which suggest less compression in the vertebrate area (thus more height, even if it is only a few millimeters) and more elasticity.

His next section about the sheep show incredible results which showed that growth plates were increased from  using recombinant OP-1. I quote this passage “”…treatment with rhOP-1 initiated a complex response that was both chondrogenic and osteogenic in nature”

The next part shows that the BMP-7/OP-1 also leads to Collagen type II and Proteoglycan synthesis increase so this protein is absolutely critical. I am willing to bet that getting the mesenchymal stem cells to differentiate into chondrocytes will only assist in the bone formation process.

Conclusion: This is one of those articles that comes out that creates a whole new pathway to look at and pushes the possibility go height increase further along. With this type of study, I am willing to bet that scientific researchers will find a way to increase height in adult within 10-15 years if they are willing to take some big risks and try a few dangerous experiments on human subjects. The next article will be a complete and full explanation of the facts and information found here. The results are amazing.

Remembering A Road Trip Through The American Midwest, A Story About Height

This is one of those stories and anecdotes that you should hear to understand just what is going on the world today, and especially of the US population in today’s modern times. This is a story about height.

About 3 and a half years ago right after I was laid off from my first corporate job after getting out of college, I found myself in one of the worst economic recessions that the US has ever seen. It was in the spring time and the leaves were finally blooming after a rather easy winter of milk weather. I decided that instead of battling it out against the other job seekers that had lost their jobs in the 2008-2009 time, I would take a road trip that I have always wanted to go on.

During my days in college, I had always wanted to go to the great midwest of the US and see what lied in that area. So about 1 week after I was laid off, I put some stuff in my car and took off for a trip that would last over 9 days, 4500 miles, and some great stories.

The path I took went like this Washington -> Idaho -> Montana – > North Dakota -> Minnesota -> Iowa -> Nebraska -> Utah -> Wyoming – > Idaho -> Oregon -> Washington.

I traveled from the west to the middle and back to the west again. In that time, I DEFINITELY noticed some major differences in the demographic of the towns and populations I passed.

The first thing I noticed is that as you go more towards the middle states, the towns move more towards the side of caucasians or native americans. In one Walmart in Minnesota, I was one of only two people who was non-caucasian. It was a very enlightening experience. The major thing I noticed about the people was that by the time I had reached the North Dakota area, the people I saw when I stopped either to use the bathroom or got gas seemed to get taller and taller.

I remember one stop I took either in North Dakota or Minnesota (probably Minnesota close to St. Cloud) where I noted that every single guy in a fast food stop was taller than me, even when I was wearing thick heeled boots. The height and size of these people were very noticeable.

I remember getting out to get gas when I drove up to Duluth, Minnesota and finding that the gas station worker was almost 6’7″. When I went to eat at a local buffet, the man who strode to the restaurant in front of me was probably a 6′ 9″ giant who didn’t seem all out of place in the city. I saw many families eating and I seemed like many of the adult men were taller than me.

When I finally left Minnesota, I drove down south to Iowa and I stopped by Cedar Springs at a local Walmart. It was there that I was greeted by a Subway Sandwich maker who was probably 6′ 8″ and I decided to sit down and just watch the people walk by. I made a specific point to note the people who were buying things and using the checkout counter. Every single man at that Walmart was taller than me, which would have put them at least 6′ 3″ or taller. I watched maybe 30 men pass through the checkout counters while I was eating my sandwich and not one was shorter than me.

When I decided to do some shopping and buy some provisions for the drive ahead, I saw who I still claim to this day is the tallest person I have ever seen in my life! 

Now, in my life I have lived in many areas of the US and I have seen my share of tall people. I have definitely seen at least 1 dozen 7 footers, once I realized that the top of most doorways in commercial building are at the 7 feet mark. I have seen many guys duck their head when they have to walk through a door way. At one point, I am almost positive I was seeing 1 footer every 6 weeks, at least last year around the Seattle area where I was living. I couldn’t understand why there was so many giants all of a sudden. It’s not like I go out a lot and see many people.

I have run in marathons before and have been to state fairs. There is always a few really tall guys but they rarely get past the 6’7″-6’8″ mark. All of a sudden last year to the beginning of this year, I started noticing that a lot of really tall 7 foot men were around.

Getting back to the story, that man I saw in a Walmart in the city of Cedar Springs Iowa was amazingly tall. I swear that from about 30 feet away, he looked like he was about 7’2-7’3″, taller than even Shaq. The even more amazing thing was that this men was slouching a lot. He looked like he was in his 70s or 80s, with a curved back, and his grandson was walking right along side of him.

I had to leave to get back to my car but I remembered just his amazing size. Everyone at that Walmart was huge but this guy who was slouching was the biggest. From far away he looked like a true giant. If he was at his prime and stood up completely straight, I would say he would probably be around the 7′ 5″-7’6″ mark. I am not joking about this.

After that incident, I never noticed many other giants on that trip. However, that one stop in Iowa has forever burned into my mind an image of what people from the Midwest are like. They are big. Now, am I going to make the statement that caucasian people are taller than other ethnicities? From my observation in that trip, I would say there is a strong correlation.

The other story I wanted to share was one time I was at a Mall in a small town in Southern Idaho. As I was walking through the mall, I noticed what appeared to be young high school boys dressed very sharply for a formal event, probably a prom or dance or something. I noted that a group of these high school boys standing in a circle and laughing at something rather childish like most High School guys (I was in college at that time so I can say something like that). In that group, it was all white caucasian guys who were all very tall, some around the 6’3″-6’4″ range, and one asian male, I would guess Chinese, who was the only short one of the group who appeared to be around 5′ 7″-5’8″.

These two stories are the only examples that I can come up from which in my memory really stood out. From just these two stories, I have sort of formed already a generalization that it really does appear that certain ethnicities or races are just taller and bigger than others, and I would guess genetics have a lot to do with it. For me, It felt like that as I drove more and more into areas of the USA where the majority of people were “white” the taller and taller the populations and people seemed to be.

I don’t know what you want to take out of this anecdotal story but maybe you found some entertainment or insight from it.

 

Brooke Greenberg Is The Girl Who Does Not Age, What Is Her Genetic Secret?

Just today while I was doing research on the fact that at least two types of animal species have been found to be biologically immortal, meaning they don’t older, I stumbled upon the story about Brooke Greenberg, who at this time is a 19 year old female but appears to have not grown older through the years. Her anthropomorphic measurements are just about 30 inches (76 cm) tall, weighs about 16 pounds (7.3 kg) which is about the usual size of a 1 year old. Her physical and mental maturity seems to not have progressed at all.

Her story was really big a few years ago when ABC News did a story on her.

From the Wikipedia article on her HERE….

Brooke Greenberg (born January 8, 1993), is an American from Reisterstown, Maryland, who has remained physically and cognitively similar to a toddler, despite her increasing age. She is about 30 inches (76 cm) tall, weighs about 16 pounds (7.3 kg), and has an estimated mental age of nine months to one year. Brooke’s doctors have termed her condition Syndrome X.

Brooke was born on January 8, 1993 at Sinai Hospital in Baltimore, Maryland, one month prior to her due date, weighing just four pounds (1.8 kg). She was born with anterior hip dislocation, a condition which caused her legs to be swiveled upwards toward her shoulders; this was corrected surgically. Otherwise, Brooke appeared to be a normal infant.

Birth and early life

In her first six years, Brooke Greenberg went through a series of unexplained medical emergencies from which she recovered. She had seven perforated stomach ulcers. She also suffered a seizure. This was followed by what was later diagnosed as a stroke; weeks later, no damage was detected. At age five, Brooke had a mass in her brain that caused her to sleep for 14 days. The doctors diagnosed the mass as a brain tumor. However, Brooke later awoke, and physicians found no tumor present. Brooke’s pediatrician, Dr. Lawrence Pakula, states that the source of her sudden illness remains a mystery.

To keep food from getting into her lungs, Brooke is fed through a permanent stomach tube. Feeding her through the tube takes ten hours a day.

Unexplained condition

Over the past several years, the Greenbergs visited many specialists, looking for an explanation for their daughter’s strange condition, yet there has been no diagnosis of any known genetic syndrome or chromosomal abnormality. In 2001, when Dateline documented Brooke, she was still the size of a six-month-old infant, weighing just 13 lb (5.9 kg) at 27 inches (69 cm) tall. The family still had no explanation. Brooke Greenberg’s mother Melanie said, “They [the specialists] just said she’ll catch up. Then we went to the nutritionist, the endocrinologist. We tried the growth hormone…”. The growth hormone treatment had no effect. Howard, Brooke’s father, said: “I mean she did not put on an ounce or she did not grow an inch … That’s when I knew there was a problem.” After the growth hormone administration failed, the doctors, unable to diagnose a known condition, named her condition Syndrome X.

The Greenbergs made many visits to nearby Johns Hopkins Children’s Center, and even took Brooke to New York’s Mount Sinai Hospital, searching for information about their daughter’s condition. When geneticists sequenced Greenberg’s DNA, they found that the genes associated with the premature aging diseases were normal, unlike the mutated versions in patients with Werner syndrome and progeria.

Medical studies

In 2006, Richard Walker, PhD in endocrine physiology of the University of South Florida College of Medicine, said that Brooke’s body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic disorder or chromosomal abnormality that would help explain why. Her telomeres seem to be shortening at the normal rate.

In 2009, Walker said: “There’ve been very minimal changes in Brooke’s brain … Various parts of her body, rather than all being at the same stage, seem to be disconnected.” Walker noted that Greenberg’s brain, for example, is not much more mature than that of a newborn infant. He estimates her mental age at around nine months to a year old. Brooke can make gestures and recognize sounds, but cannot speak. Her bones are like those of a ten-year-old, and she still has her baby teeth, which have an estimated developmental age of about eight years. Said Walker, “We think that Brooke’s condition presents us with a unique opportunity to understand the process of aging.”  “Different parts of her body are developing at different rates, as if they were not a unit but parts of separate organisms,” Walker explains.

Dr. Walker believes that the condition resulted from a failure of central control genes. He has identified two more people with similar developmental issues: Gabrielle Williams of Montana (born 2004) and Nicky Freeman of Australia (born 1970), a forty-year-old man who looks like a boy. Others, such as British biologist Aubrey de Grey, believe that aging and development are not related.

Me: What is fascinating about this story is that even the geneticists are perplexed by wha they are seeing. this girl is not suffering from the ordinary genetic issues like Werner syndrome or progeria. It states that “She has never been diagnosed with any known genetic disorder or chromosomal abnormality that would help explain why. Her telomeres seem to be shortening at the normal rate.” It would appear that she is growing and gaining weight and may be going through the process but the rate at which she is aging and changing is extremely slow. The incident where she developed a brain tumor that went away after a few weeks is ridiculous. At the end of the wikipedia article, I noted the statement that “aging and development are not related”. That is definitely a challenged to what most people would think is so self evident that is common sense but from a scientific point of view makes sense. Aging and development don’t always have to go together, it may just appear from the outside in a phenotypical way to be the same thing. Maybe there are people like Brooke which do age, but don’t develop. They even did a documentary on her entitled ‘Girl Frozen In Time” that aired on TLC.

As for any height increase related news, the doctors did try to put her on a growth hormone therapy but she didn’t gain any height or even weight. Now that is ridiculous. They stated that her body is not developing at the same rate, but separately. 

From ABC News 20/20 website HERE

Doctors Baffled, Intrigued by Girl Who Doesn’t Age

By BOB BROWN
June 23, 2009

Brooke Greenberg is the size of an infant, with the mental capacity of a toddler.

She turned 16 in January.

“Why doesn’t she age?” Howard Greenberg, 52, asked of his daughter. “Is she the fountain of youth?”

Such questions are why scientists are fascinated by Brooke. Among the many documented instances of children who fail to grow or develop in some way, Brooke’s case may be unique, according to her doctor, Johns Hopkins School of Medicine pediatrician Lawrence Pakula, in Baltimore.

“Many of the best-known names in medicine, in their experience … had not seen anyone who matched up to Brooke,” Pakula said. “She is always a surprise.”

Brooke hasn’t aged in the conventional sense. Dr. Richard Walker of the University of South Florida College of Medicine, in Tampa, says Brooke’s body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic syndrome or chromosomal abnormality that would help explain why.

In a recent paper for the journal “Mechanisms of Ageing and Development,” Walker and his co-authors, who include Pakula and All Children’s Hospital (St. Petersburg, Fla.) geneticist Maxine Sutcliffe chronicled a baffling range of inconsistencies in Brooke’s aging process. She still has baby teeth at 16, for instance. And her bone age is estimated to be more like 10 years old.

“There’ve been very minimal changes in Brooke’s brain,” Walker said. “Various parts of her body, rather than all being at the same stage, seem to be disconnected.”

Brooke’s mother, Melanie Greenberg, 48, sees a different picture. “She loves to shop,” Greenberg said. “Just like a woman.”

Brooke rides in a stroller while her mom shops for clothes in the infant sections of department stores near their home in a Baltimore suburb. That Brooke is in her mid-teens is so mind-boggling that if another mother with a toddler asks Greenberg how old Brooke is, she usually doesn’t try to explain.

“My system always has been to turn years into months,” Greenberg said. “So, if someone asked today, I might say, she’s 16 months old.”

The Toddler Who Rebels Like a Teen

Brooke weighs 16 pounds and is 30 inches tall. She doesn’t speak, but she laughs when she is happy, and she clearly recognizes the people around her. She has three sisters: Emily, 22; Caitlin, 19; and Carly, 13. All three are bright, active and of normal size and development. They say that Brooke has ways of expressing herself like the teenager she is.

“She looks like a 6-month-old, but she kind of has a personality of a 16-year-old,” Caitlin said. “Sometimes we joke about how she rebels.”

Brooke will resist and refuse activities that don’t appeal to her by vocalizing her displeasure, not with words, but with sounds typical of an infant. “She makes it known what she likes and what she doesn’t like,” sister Emily said.

Carly said it no longer seems strange to have an older sister who is still essentially an infant. “As I got older, she was just like another little sister to me,” she said.

In her first six years, Brooke went through a series of medical emergencies from which she recovered, often without explanation. She survived surgery for seven perforated stomach ulcers. She suffered a brain seizure followed by what was diagnosed as a stroke that weeks later left no apparent damage.

Page 2 of 3

June 23, 2009

At 4, she fell into a lethargy that caused her to sleep for 14 days. Then, doctors diagnosed a brain tumor, and the Greenbergs bought a casket for her.

“We were preparing for our child to die,” Howard Greenberg said. “We were saying goodbye. And, then, we got a call that there was some change; that Brooke had opened her eyes and she was fine. There was no tumor. She overcomes every obstacle that is thrown her way.”

Brooke’s doctor said the source of her sudden illnesses remains a mystery.

“We often did not have a good explanation for why she became ill as quickly and intensely as she did,” Pakula said. “There were many times in which there were real doubts about her ability to survive.”

As she rocks back and forth in a baby swing, Brooke is fed through a tube inserted into her stomach, because her esophagus is so small that swallowed food could back up into her lungs and cause pneumonia.

Doctors recommended growth hormone therapy early in Brooke’s life, but the treatment produced no results.

Howard Greenberg recalled the follow-up visit to the endocrinologist. “We took her back in six months, and the doctor looked at us and said, ‘Why didn’t you give Brooke the growth hormones?’ And I said, ‘We gave Brooke the growth hormones. We gave her everything you told us to do.’ And Brooke didn’t put on a pound, an ounce; she didn’t grow an inch.”

Part of the Family

Brooke’s hair and her nails are the only two things that grow, Howard said. “She has pajamas and outfits that are 10 or 12 years old,” he said.

One of the things she loves most is movement. As Brooke lies on her stomach, Carly often steers her through the house on an ottoman. Brooke also likes to push against open kitchen drawers until they slam shut.

In her crib, “she’s very content,” Howard said. “She has very little conception of time.”

The family has placed a small television near the crib so she can watch whenever she pleases. Her father gets up in the middle of each night to check on her.

Brooke has a caretaker during daytime hours, but the family’s schedule revolves around her, year after year. The Greenbergs take no vacations, have few nights out and involve Brooke in as many family activities as possible.

“To go to a swimming pool for the summer, or belong to a summer club … we tried all those things, and it’s lacking something,” her mother said. “Brooke’s not there. We’re not a family without Brooke.”

Brooke goes to a Baltimore County public school, Ridge Ruxton, dedicated to special education. Based on her age, she would be a junior in high school. Jewel Adiele, one of Brooke’s teachers, said she wonders sometimes what Brooke is thinking or perceiving.

“People who have worked with her in the past or who briefly see her say … there’s no change,” Adiele said. “But I think, in her heart, she changes. I think from day to day, there are changes. They’re not just as visible as you see in a lot of teens.”

To try to determine why Brooke’s aging process has been so irregular — and what it means to the understanding of our genetic makeup — Walker and Sutcliffe have studied samples of Brooke’s cells and DNA to look for what they think may be a genetic mutation never seen before that has affected the way she ages.

Walker, of the University of South Florida, believes that if the gene can be isolated, it may provide clues to questions about why we age and die.

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June 23, 2009

“Without being sensational, I’d say this is an opportunity for us to answer the question, why we’re mortal, or at least to test it,” Walker said. “And if we’re wrong, we can discard it. But if we’re right, we’ve got the golden ring.”

A Key to Understanding How We Age?

If the gene — or complex of genes — is identified, Walker plans to test laboratory animals to determine whether the gene can be switched off and, if so, whether it will cause the animal’s aging to slow.

In the long term, the idea that the aging process might somehow be manipulated raises serious questions about what human beings might do with that knowledge.

“Clearly, that’s the science fiction aspect of it,” said Walker, describing the social and ethical dilemmas that would arise. “We can’t have continued reproduction and people who don’t age.”

One possible reason to slow the aging process, Walker suggested, would be to allow astronauts to travel in space for long periods of time. “But right now, it’s only conjecture,” he said.

Neither Walker nor Pakula, her doctor, can speculate how long Brooke’s life might be. “That’s more of a crystal ball question,” Pakula said. “I think there’s no way of knowing. ”

The visual evidence of that unpredictable future is always there in the family pictures — photographs in which everyone but Brooke is aging.

The Greenbergs are fascinated by the promise that a scientific breakthrough may stem from Brooke, whose own life is governed by the most basic elements: food and shelter; a family’s love; and their ability to see in her far more than meets the eye, having come to terms with the prospect that she will never grow up.

“We love her just the way she is,” Melanie Greenberg said. “We don’t want to change her.”

Added Howard Greenberg, “Brooke is the nucleus of our family. What if Brooke holds the secret to aging? We’d like to find out. We’d like to help people. Everybody’s here for a reason. Maybe this is why Brooke is here.”

For more of Brooke’s story, watch the documentary, “Child Frozen In Time,” Sunday, Aug. 9 at 10 p.m. on TLC.

Increase Height And Grow Taller Using Letrozole And Anastrozole

Something I have read about in the Giant Scientific forum and the Impartial Height Board discussion was the talk of using other types of steroid to possibly inhibit the aromitization factor of estrogen just like previously looked at compounds like anavar. I know at least one person who decided to incorporate these compounds into their routine as a type of multivitamin supplement to possibly increase the GH release rate or slow down the rate of growth plate senescence.

this next part was taking from the Anabolic Minds forums located HERE, on the same post where people talked about the possibility of using GHenerate and I-GH-1 in possibly increasing height.

rms80

Running with the Big BoysBoard Sponsor

Originally Posted by BeastMode View Post
Im 18, will HGH make me any taller? I heard that it will. Is this fact or fiction?

Thought you guys might find this interesting- a little food for thought:

in Endocrinol (Oxf). 2006 May;64(5):510-3. Treatment with the aromatase inhibitor letrozole during adolescence increases near-final height in boys with constitutional delay of puberty.

Hero M, Wickman S, Dunkel L.
Source

Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland.

Abstract

OBJECTIVE:

We investigated whether inhibition of oestrogen biosynthesis with the aromatase inhibitor, letrozole, during adolescence improves near-final height in boys with constitutional delay of puberty.

PATIENTS AND METHODS:

Seventeen boys with constitutional delay of puberty were randomized to receive testosterone (T) enanthate (1 mg/kg i.m.) every 4 weeks for 6 months in combination with placebo (Pl, n = 8), or the aromatase inhibitor letrozole (Lz, 2.5 mg/day orally) (n = 9), for 12 months. After treatment, patients were followed up until near-final height. Height discrepancy was calculated as near-final height minus mid-parental target height.

MEASUREMENTS:

The primary end point was the difference in near-final height between the groups treated either with T + Pl or T + Lz. Secondarily, height discrepancy and gain in height standard deviation score (SDS) were analysed in both groups.

RESULTS:

Boys treated with T + Lz reached a higher mean near-final height than did boys on T + Pl (175.8 vs. 169.1 cm, respectively, P = 0.04). In T + Lz-treated boys, mean near-final height did not differ from their mid-parental target height (175.8 vs. 177.1 cm, P = 0.38), whereas in T + Pl-treated boys, mean near-final height was lower than mid-parental target height (169.1 vs. 173.9 cm, P = 0.007). T + Lz-treated boys had a greater increment in height SDS over the pretreatment height SDS than T + Pl-treated boys (+1.4 SDS vs.+0.8 SDS, P = 0.03).
CONCLUSIONS:

Our findings indicate that in adolescent boys an increase in adult height can be attained by use of aromatase inhibitors.

J Clin Endocrinol Metab. 2005 Dec;90(12):6396-402. Epub 2005 Sep 27.
Inhibition of estrogen biosynthesis with a potent aromatase inhibitor increases predicted adult height in boys with idiopathic short stature: a randomized controlled trial.

Hero M, Norjavaara E, Dunkel L.

Source

Hospital for Children and Adolescents, University of Helsinki, Finland.

Abstract

CONTEXT:

In males as well as in females, estrogen is an essential regulator of bone maturation, growth plate fusion, and cessation of longitudinal growth. Therefore, an increase in predicted adult height (PAH) may be achieved in short boys by blocking estrogen biosynthesis.

OBJECTIVE:

We tested the hypothesis that a decrease in the rate of bone maturation and an increase in PAH can be achieved in boys with idiopathic short stature (ISS) by the method of blocking estrogen biosynthesis with an aromatase inhibitor. Secondarily, we investigated the effects of aromatase inhibition on bone mineralization.
DESIGN:

This was a prospective, double-blind, randomized, placebo (Pl)-controlled clinical study.
SETTING:

The study was performed at a university hospital out-patient clinic.
PATIENTS:

Thirty-one boys, aged 9.0-14.5 yr, with ISS were studied.
INTERVENTION:

The boys were treated with the aromatase inhibitor letrozole (Lz; 2.5 mg/d) or Pl for 2 yr.
MAIN OUTCOME MEASURE:

The main outcome measure was the change in PAH after 24 months of treatment.
RESULTS:

PAH increased by 5.9 cm (P < 0.0001), and height SD score for bone age increased by 0.7 SD score (P < 0.0001) in the Lz-treated boys, whereas no changes occurred in the respective measures in Pl-treated boys. Areal bone mineral density of the lumbar spine and femoral neck, assessed by dual-energy x-ray absorptiometry, increased in a similar fashion in both groups during the treatment, whereas bone mineral apparent density increased only in those taking Lz (median increase, 4.3%; P = 0.009).
CONCLUSIONS:

Treatment with the aromatase inhibitor Lz delays bone maturation and improves PAH in boys with ISS. No adverse effects on bone mineralization were evident after 2 yr of treatment.

J Clin Endocrinol Metab. 2008 Mar;93(3):823-31. Epub 2007 Dec 28.

Anastrozole increases predicted adult height of short adolescent males treated with growth hormone: a randomized, placebo-controlled, multicenter trial for one to three years.

Mauras N, Gonzalez de Pijem L, Hsiang HY, Desrosiers P, Rapaport R, Schwartz ID, Klein KO, Singh RJ, Miyamoto A,Bishop K.
Source

Nemours Children’s Clinic, Division of Endocrinology, 807 Children’s Way, Jacksonville, Florida 32207, USA.nmauras@nemours.org

Abstract

CONTEXT:

The process of epiphyseal fusion during puberty is regulated by estrogen, even in males.
OBJECTIVE:

Our objective was to investigate whether anastrozole, a potent aromatase inhibitor, could delay bone age acceleration and increase predicted adult height in adolescent boys with GH deficiency.
METHODS:

Fifty-two adolescent males with GH deficiency treated with GH were randomized to cotreatment with anastrozole or placebo daily for up to 36 months.
RESULTS:

Fifty subjects completed 12 months, 41 completed 24 months, and 28 completed 36 months. Linear growth was comparable between groups; however, there was a significantly slower increase in bone age advancement from baseline in the anastrozole group vs. placebo group after 2 yr (+1.8+/-0.1 vs. +2.7+/-0.1 yr, P<0.0001) and after 3 yr (+2.5+/-0.2 vs. +4.1+/-0.1 yr, P<0.0001). This resulted in a net increase in predicted adult height of +4.5+/-1.2 cm in the anastrozole group at 24 months and +6.7+/-1.4 cm at 36 months as compared with a 1-cm gain at both time points in the placebo group. Estradiol and estrone concentrations increased less in the anastrozole group compared with placebo group. All boys on the aromatase inhibitor had normal tempo of virilization. Safety data, including glucose, and plasma lipid concentrations were comparable between groups.

CONCLUSIONS:

Anastrozole increases adult height potential of adolescent boys on GH therapy while maintaining normal pubertal progression after 2-3 yr. This treatment offers an alternative in promoting growth in GH-deficient boys in puberty. Long-term follow up is needed to elucidate fully the safety and efficacy of this approach.

Dirk Tanis, BA, MSci
Chief Operating Officer, Applied Nutriceuticals
Conclusion: It really does appear that any type of steroids that like the aromatase inhibitor letrozole and Anastrozole during  used during adolescence will work in increasing the final height of the still growing individuals. They somehow slow down the age of puberty and full bone maturation.